Cardiovascular disease (CVD) is the leading cause of death in western countries. Atherosclerosis is a condition involving the accumulation of lipid-rich plaques and chronic inflammation of the vascular wall. Plaque deposits initiate when low-density lipoproteins (LDL) accumulate in the artery wall and subsequently undergo oxidative modification (oxLDL). OxLDL stimulates endothelial inflammation triggering monocyte recruitment and subsequent monocyte differentiation to macrophages. Intimal macrophages exhibit unregulated uptake of oxLDL, via scavenger receptors, leading to the formation and accumulation of lipid laden macrophages (foam cells), which in turn drives plaque development. Class A and B scavenger receptors account for 75 to 90% uptake of modified LDLs. Development of a targeted and shielded therapeutic for managing atherosclerosis is needed.